Our overall objective is to study the pathogenesis of corneal edema which occurs following intraocular surgery. Clinically, following cataract, vitrectomy and anterior segment surgery, and increase in corneal thickness and a loss of endothelial cells occur. The increase in thickness is either the result of an increase in stromal water and/or the loss of stromal proteoglycans and glycoproteins resulting from a loss of the corneal endothelial barrier and/or pump function. The following studies should further our understanding and treatment of postsurgical corneal edema. The specific aims of this proposal are: (1) To determine what role corneal endothelial Na+/K+ ATPase has in corneal deturgescense. The Na+/K+ ATPase density as measured by ouabain binding will be studied in rabbit, cat and human, and the density (pump function) will be correlated to age, regeneration and ouabain inhibition. (2) To determine the role of corneal endothelial membrane proteins in the maintenance of the endothelial barrier function. The major endothelial membrane proteins will be determined by SDS-PAGE electrophoresis in bovine, rabbit and human in a controlled endothelium and following barrier disruption. (3) To correlate the morphology of the edematous corneal stroma to the loss of stromal proteoglycans, glycoproteins and the aggregation of collagen fibrils. (4) To determine the effects of surgical procedures (epithelial debridement, radial keratotomy, cataract surgery) and drugs (benzalkonium chloride and carbonic anhydrase inhibitors) on the corneal endothelial barrier and pump function. (5) To measure the stromal soluble proteins, proteoglycans and glycoproteins of the non-swelling elasmobranch cornea and the non-fused stroma of the marine teleost cornea.